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Distinct roles of complement receptor 3, Dectin-1, and sialic acids in murine macrophage interaction with Histoplasma
Jr-Shiuan Lin1, Juin-Hua Huang, Li-Yin Hung
1Graduate Institute of Immunology, National Taiwan University College of Medicine, Taipei, Taiwan.
Abstract:
The yeast cells of dimorphic fungal pathogen Histoplasma reside primarily within the macrophages of an infected host; the interaction between the yeast and macrophage has a profound impact on host defense against the fungus. We used blocking antibodies and saccharides to identify the receptors that participate in the phagocytosis of and the cytokine response to Histoplasma. The phagocytosis and cytokine response results show that sialic acids on the macrophages were involved in the interaction between macrophages and Histoplasma. CR3, although not the only receptor involved, was responsible for phagocytosis and cytokine response. It is unclear which receptors other than CR3 are responsible for phagocytosis, but we did rule out the participation of TLR2, TLR4, MR, DC-SIGN/SIGNR1, FcgammaR, VLA-5, and Dectin-1. Even though Dectin-1 did not participate in phagocytosis, it collaborated with CR3 in the cytokine response to Histoplasma, suggesting that in the presence of phagocytic receptors, Histoplasma triggers cytokine signals through Dectin-1. Moreover, macrophage phagocytosis of and cytokine response to Histoplasma are Syk kinase-dependent. Our study delineated the distinct roles of CR3, Dectin-1, and sialic acids in the interaction with Histoplasma and suggested that multiple receptor use might be important to host defense against Histoplasma.
Insights
Host defense against Histoplasma involves macrophage interactions. Sialic acids and complement receptor 3 (CR3) mediate fungal uptake and cytokine release, with Dectin-1 collaborating in cytokine signaling.
Area of Science:
- Immunology
- Mycology
- Cell Biology
Background:
- The dimorphic fungal pathogen Histoplasma yeast resides within host macrophages, influencing host defense.
- Understanding macrophage-fungal interactions is crucial for developing effective antifungal strategies.
Purpose of the Study:
- To identify specific macrophage receptors involved in the phagocytosis and cytokine response to Histoplasma.
- To elucidate the roles of identified receptors in host defense mechanisms against Histoplasma infection.
Main Methods:
- Utilized blocking antibodies and saccharides to probe receptor-ligand interactions.
- Assessed phagocytosis rates and cytokine production following macrophage-Histoplasma co-incubation.
- Investigated the involvement of various known immune receptors, including CR3, TLR2, TLR4, MR, DC-SIGN/SIGNR1, FcgammaR, VLA-5, and Dectin-1.
Main Results:
- Sialic acids on macrophages are implicated in the interaction with Histoplasma.
- Complement receptor 3 (CR3) plays a significant role in both phagocytosis and cytokine response.
- Dectin-1 collaborates with CR3 in mediating cytokine responses, independent of phagocytosis, and signaling is Syk kinase-dependent.
Conclusions:
- Distinct roles for CR3, Dectin-1, and sialic acids in Histoplasma recognition and host response were delineated.
- Multiple receptor engagements are likely essential for robust host defense against Histoplasma.
- Targeting these specific receptors could offer novel therapeutic avenues for histoplasmosis.
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